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dc.contributor.author | Kobayashi, Junya | en |
dc.contributor.author | Fujimoto, Hiroko | en |
dc.contributor.author | Sato, Jun | en |
dc.contributor.author | Hayashi, Ikue | en |
dc.contributor.author | Burma, Sandeep | en |
dc.contributor.author | Matsuura, Shinya | en |
dc.contributor.author | Chen, David J | en |
dc.contributor.author | Komatsu, Kenshi | en |
dc.contributor.alternative | 小林, 純也 | ja |
dc.date.accessioned | 2012-12-04T05:57:47Z | - |
dc.date.available | 2012-12-04T05:57:47Z | - |
dc.date.issued | 2012-11-07 | - |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | http://hdl.handle.net/2433/162961 | - |
dc.description.abstract | H2AX is an important factor for chromatin remodeling to facilitate accumulation of DNA damage-related proteins at DNA double-strand break (DSB) sites. In order to further understand the role of H2AX in the DNA damage response (DDR), we attempted to identify H2AX-interacting proteins by proteomics analysis. As a result, we identified nucleolin as one of candidates. Here, we show a novel role of a major nucleolar protein, nucleolin, in DDR. Nucleolin interacted with γ-H2AX and accumulated to laser micro-irradiated DSB damage sites. Chromatin Immunoprecipitation assay also displayed the accumulation of nucleolin around DSB sites. Nucleolin-depleted cells exhibited repression of both ATM-dependent phosphorylation following exposure to γ-ray and subsequent cell cycle checkpoint activation. Furthermore, nucleolin-knockdown reduced HR and NHEJ activity and showed decrease in IR-induced chromatin accumulation of HR/NHEJ factors, agreeing with the delayed kinetics of γ-H2AX focus. Moreover, nucleolin-knockdown decreased MDC1-related events such as focus formation of 53 BP1, RNF168, phosphorylated ATM, and H2A ubiquitination. Nucleolin also showed FACT-like activity for DSB damage-induced histone eviction from chromatin. Taken together, nucleolin could promote both ATM-dependent cell cycle checkpoint and DSB repair by functioning in an MDC1-related pathway through its FACT-like function. | en |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.rights | © 2012 Kobayashi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. | en |
dc.title | Nucleolin Participates in DNA Double-Strand Break-Induced Damage Response through MDC1-Dependent Pathway. | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.jtitle | PloS one | en |
dc.identifier.volume | 7 | - |
dc.identifier.issue | 11 | - |
dc.relation.doi | 10.1371/journal.pone.0049245 | - |
dc.textversion | publisher | - |
dc.identifier.artnum | e49245 | - |
dc.identifier.pmid | 23145133 | - |
dcterms.accessRights | open access | - |
出現コレクション: | 学術雑誌掲載論文等 |
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